High-sensitivity troponin T, NT-proBNP and glomerular filtration rate: A multimarker strategy for risk stratification in chronic heart failure

Alberto Aimo, James L. Januzzi, Giuseppe Vergaro, Andrea Ripoli, Roberto Latini, Serge Masson, Michela Magnoli, Inder S. Anand, Jay N. Cohn, Luigi Tavazzi, Gianni Tognoni, Jørgen Gravning, Thor Ueland, Ståle H. Nymo, Hans Peter Brunner La Rocca, Antoni Bayes-Genis, Josep Lupón, Rudolf A. de Boer, Akiomi Yoshihisa, Yasuchika TakeishiMichael Egstrup, Ida Gustafsson, Hanna K. Gaggin, Kai M. Eggers, Kurt Huber, Ioannis Tentzeris, W. H. Wilson Tang, Justin L. Grodin, Claudio Passino, Michele Emdin

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Background: In a recent individual patient data meta-analysis, high-sensitivity troponin T (hs-TnT) emerged as robust predictor of prognosis in stable chronic heart failure (HF). In the same population, we compared the relative predictive performances of hs-TnT, N-terminal fraction of pro-B-type natriuretic peptide (NT-proBNP), hs-C-reactive protein (hs-CRP), and estimated glomerular filtration rate (eGFR) for prognosis. Methods and results: 9289 patients (66 ± 12 years, 77% men, 85% LVEF <40%, 60% ischemic HF) were evaluated over a 2.4-year median follow-up. Median eGFR was 58 mL/min/1.73 m2 (interquartile interval 46–70; n = 9220), hs-TnT 16 ng/L (8–20; n = 9289), NT-proBNP 1067 ng/L (433–2470; n = 8845), and hs-CRP 3.3 mg/L (1.4–7.8; n = 7083). In a model including all 3 biomarkers, only hs-TnT and NT-proBNP were independent predictors of all-cause and cardiovascular mortality and cardiovascular hospitalization. hs-TnT was a stronger predictor than NT-proBNP: for example, the risk for all-cause death increased by 54% per doubling of hs-TnT vs. 24% per doubling of NT-proBNP. eGFR showed independent prognostic value from both hs-TnT and NT-proBNP. The best hs-TnT and NT-proBNP cut-offs for the prediction of all-cause death increased progressively with declining renal function (eGFR ≥ 90: hs-TnT 13 ng/L and NT-proBNP 825 ng/L; eGFR < 30: hs-TnT 40 ng/L and NT-proBNP 4608 ng/L). Patient categorization according to these cut-offs effectively stratified patient prognosis across all eGFR classes. Conclusions: hs-TnT conveys independent prognostic information from NT-proBNP, while hs-CRP does not. Concomitant assessment of eGFR may further refine risk stratification. Patient classification according to hs-TnT and NT-proBNP cut-offs specific for the eGFR classes holds prognostic significance.

Original languageEnglish (US)
Pages (from-to)166-172
Number of pages7
JournalInternational Journal of Cardiology
Volume277
DOIs
StatePublished - Feb 15 2019

Bibliographical note

Funding Information:
Dr. Januzzi has received grant support from Siemens, Singulex, and Prevencio; consulting income from Roche Diagnostics, Critical Diagnostics, Philips, and Novartis; and participates in clinical end point committees for Novartis, Amgen, Janssen, and Boehringer Ingelheim. Dr. Latini and Dr. Masson have received grant support and travel reimbursements from Roche Diagnostics. Dr. Tavazzi reports personal fees from Servier, personal fees from CVIE Therapeutics, outside the submitted work. Dr. Gravning reports lecture fees from AstraZeneca, Siemens and Abbott Laboratories, outside the submitted work. Dr. Brunner-La Rocca reports unrestricted research grants and consulting fees from Roche Diagnostics, as well as unrestricted research grants from Novartis and Vifor outside this work. Dr. Bayes-Genis has received grant support from Roche Diagnosis, lecture honoraria from Roche Diagnostics and Critical Diagnostics, and consulting income from Roche Diagnostics, Critical Diagnostics, and Novartis. Dr. Lup?n has received lecture honoraria from Roche Diagnostics. Dr. de Boer reports that Roche, Novartis, and AstraZeneca offered consultancy to UMCG; he also reports grants from AstraZeneca, grants from Bristol Myers Squibb, and grants from Trevena, outside the submitted work. Dr. Gustafsson reports personal fees from Boehringer-Ingelheim, personal fees from Novo Nordisk, personal fees from Novartis, personal fees from MSD, personal fees from Astra-Zeneca, outside the submitted work. Dr. Gaggin has received grant support from Roche and Portola; consulting income from Roche Diagnostics, Amgen and Ortho Clinical; research payments for clinical endpoint committees for EchoSense and Radiometer. Dr. Eggers has received honoraria from Abbott Laboratories and AstraZeneca, and has served as a consultant for Abbott Laboratories and Fiomi Diagnostics. Dr. Tang reports grants from National Institutes of Health, outside the submitted work. All disclosed relationships are modest. All other Authors have nothing to disclose.

Funding Information:
Dr. Januzzi has received grant support from Siemens , Singulex , and Prevencio ; consulting income from Roche Diagnostics, Critical Diagnostics, Philips, and Novartis; and participates in clinical end point committees for Novartis, Amgen, Janssen, and Boehringer Ingelheim. Dr. Latini and Dr. Masson have received grant support and travel reimbursements from Roche Diagnostics. Dr. Tavazzi reports personal fees from Servier, personal fees from CVIE Therapeutics, outside the submitted work. Dr. Gravning reports lecture fees from AstraZeneca, Siemens and Abbott Laboratories, outside the submitted work. Dr. Brunner-La Rocca reports unrestricted research grants and consulting fees from Roche Diagnostics, as well as unrestricted research grants from Novartis and Vifor outside this work. Dr. Bayes-Genis has received grant support from Roche Diagnosis, lecture honoraria from Roche Diagnostics and Critical Diagnostics, and consulting income from Roche Diagnostics, Critical Diagnostics, and Novartis. Dr. Lupón has received lecture honoraria from Roche Diagnostics. Dr. de Boer reports that Roche, Novartis, and AstraZeneca offered consultancy to UMCG; he also reports grants from AstraZeneca, grants from Bristol Myers Squibb, and grants from Trevena, outside the submitted work. Dr. Gustafsson reports personal fees from Boehringer-Ingelheim, personal fees from Novo Nordisk, personal fees from Novartis, personal fees from MSD, personal fees from Astra-Zeneca, outside the submitted work. Dr. Gaggin has received grant support from Roche and Portola; consulting income from Roche Diagnostics, Amgen and Ortho Clinical; research payments for clinical endpoint committees for EchoSense and Radiometer. Dr. Eggers has received honoraria from Abbott Laboratories and AstraZeneca, and has served as a consultant for Abbott Laboratories and Fiomi Diagnostics. Dr. Tang reports grants from National Institutes of Health, outside the submitted work. All disclosed relationships are modest. All other Authors have nothing to disclose.

Publisher Copyright:
© 2018 Elsevier B.V.

Keywords

  • Heart failure
  • Prognosis
  • Renal function
  • Troponin

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